The major objective of this research proposal is to study the Starling forces i.e. (tissue pressure, capillary pressure, tissue colloid osmotic pressure, capillary osmotic pressure and lymph flow) and the permeability properties of the pulmonary exchange vessels during the formation of pulmonary edema induced by increased hydrostatis pressure. An in situ dog lung can be continuously weighed and arterial and venous pressures can be controlled at any desired level. A small lymphatic vessel will also be cannulated to measure flow and lymph protein as capillary pressure is elevated. Capillary pressure will be elevated in steps of 5 mm Hg and the capillary filtration coefficient, lymphatic protein flux (lymph flow times lymph protein concentration), tissue fluid pressure (as measured by implanted capsules and small fluid filled airways), capillary pressure and lymph and plasma colloid osmotic pressure (measured using a membrane osmometer) will be evaluated at each new steady state obtained by the lung. The permeability characteristics of the pulmonary exchange vessels can be assessed at each pressure level by estimating the reflection coefficient and permeability surface area products of 7 different protein fractions in lymph. In addition, the osmotic transient approach will be used an additional estimate of capillary permeability. By combining an analysis of Starling forces changes with capillary permeability measurements, we will be able to build a more comprehensive model of the development of pulmonary edema caused by other agents such as histamine, serotonin, etc.